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A. Polosa, A. Dorfman, F. Costescu, J. Racine, S. Chemtob, P. Lachapelle; Postnatal Hyperoxia in Rats: mfVEPs Uncover Islands of Normal and Abnormal Visual Function. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4062.
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© ARVO (1962-2015); The Authors (2016-present)
Previous studies have shown that postnatal hyperoxic exposure causes a severe pan-retinal disorder with retinal areas of normalcy (mfERGs). The purpose of this study was to determine whether a similar mosaic could be observed at the visual cortex.
Newborn Sprague Dawley (SD) and Long Evans (LE) rats were exposed (from P0-6, P6-14, and P0-14) to 80% O2 and compared to rats raised in normoxia. mfERGs and mfVEPs were recorded quasi-simultaneously at P60 [VERIS 4.8; camera display unit, 1 and 37 hexagon (hx) matrices; white: 200cd.m-2; black: 0cd.m-2; background: 100cd.m2; bandwidth: 10-100 Hz] with 4-minute m-sequences (interframe interval: 13.3ms). Data analysis was limited to the first order kernel.
mfERG summed responses of the 37hx showed significant (p<.05) amplitude attenuations for P6-14 and P0-14 exposures [49±27% and 78±55% (SD) and 76±6% and 59±21% (LE) of control respectively]. The most prominent component of the mfVEP response (P3) also showed a significant (p<.05) decrease in amplitude following P6-14 and P0-14 exposures to 55±43% and 45±6% (SD) and 74±44% and 57±48% (LE) of control, respectively. Analysis of individual mfVEP responses revealed that the anomalies involved mostly the superior hx of the mfVEP stimulus in SD rats, while in LE rats they were equally distributed across the entire array. In comparison, individual mfERG responses evoked from the central and inferior retinas were most affected in LE and SD rats. Of interest, a strong correlation was found between the mfERG responses (1 and 37hx) and the mfVEP P3 value obtained with the same matrices (SD: r2: 0.64 and 0.88 and LE: r2: 0.89 and 0.83, respectively).
Our results thus strongly suggest that the retinopathy that results from postnatal exposure to a hyperoxic environment causes severe and (presumably) irreversible cortical damages that appear to be distributed in a fashion that could suggest a retinotopic organisation. However it remains to be determined how much of the cortical effect we report can be accounted for by the retinopathy. These anomalies are most severe in the LE rat model a finding that points once more to the increased susceptibility of this strain for postnatal oxidative stresses.
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